BACKGROUND: Ethanol may increase the production of reactive oxygen species (ROS) in the liver, which results in the development of alcoholic liver disease (ALD). Cytokine-activated blood leukocytes may also participate in this process. The aim of our study was to evaluate the oxidative stress level in the blood of patients with alcoholic liver cirrhosis. MATERIAL/ METHODS: Blood neutrophils from 16 patients with compensated alcoholic liver cirrhosis and 28 patients with decompensated were evaluated for their ability to produce superoxide anion and hydrogen peroxide spontaneously and after PMA induction, in comparison to controls (16 healthy persons). Serum catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx) activity were also measured in both groups of patients and in the controls. RESULTS: The neutrophils from patients with compensated liver cirrhosis spontaneously produced a normal level of O2*- and a high level of H2O2, but exhibited a defect in PMA-induced O2*- production. The neutrophils from patients with decompensated liver cirrhosis spontaneously produced more O2*- and H2O2 than the controls, but the PMA response was weak. There were no changes in the expression of GPx, but enhanced SOD activity was observed in the serum of patients with decompensated alcoholic liver cirrhosis. Increased CAT activity was detected only in serum from patients with compensated liver cirrhosis. CONCLUSIONS: These data point to oxidative stress in the blood of patients with decompensated alcoholic cirrhosis, since increased resting production of ROS in neutrophils was not accompanied by increased GPx and CAT activity in serum.
BACKGROUND:Ethanol may increase the production of reactive oxygen species (ROS) in the liver, which results in the development of alcoholic liver disease (ALD). Cytokine-activated blood leukocytes may also participate in this process. The aim of our study was to evaluate the oxidative stress level in the blood of patients with alcoholic liver cirrhosis. MATERIAL/ METHODS: Blood neutrophils from 16 patients with compensated alcoholic liver cirrhosis and 28 patients with decompensated were evaluated for their ability to produce superoxide anion and hydrogen peroxide spontaneously and after PMA induction, in comparison to controls (16 healthy persons). Serum catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx) activity were also measured in both groups of patients and in the controls. RESULTS: The neutrophils from patients with compensated liver cirrhosis spontaneously produced a normal level of O2*- and a high level of H2O2, but exhibited a defect in PMA-induced O2*- production. The neutrophils from patients with decompensated liver cirrhosis spontaneously produced more O2*- and H2O2 than the controls, but the PMA response was weak. There were no changes in the expression of GPx, but enhanced SOD activity was observed in the serum of patients with decompensated alcoholic liver cirrhosis. Increased CAT activity was detected only in serum from patients with compensated liver cirrhosis. CONCLUSIONS: These data point to oxidative stress in the blood of patients with decompensated alcoholic cirrhosis, since increased resting production of ROS in neutrophils was not accompanied by increased GPx and CAT activity in serum.
Authors: Thomas H Frazier; Abigail M Stocker; Nicole A Kershner; Luis S Marsano; Craig J McClain Journal: Therap Adv Gastroenterol Date: 2011-01 Impact factor: 4.409